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ORIGINAL RESEARCH
275
Address for correspondence: Raj Kumar, MD, Department of Respiratory Allergy and Applied Immunology National Centre of Respiratory Allergy, Asthma and Immunology,
V P Chest Institute, University of Delhi, Delhi 110007, India, Tel.: 9810146835; 91-011-27667667 Ext. 144; Fax: 91-011-27667420; e-mail: rajkumarvpci@gmail.com
DOI: 10.5603/PiAP.2015.0047
Received: 17.12.2014
Copyright © 2015 PTChP
ISSN 0867–7077
Raj Kumar1, Jitendra K. Nagar2, Nitin Goel1, Pawan Kumar2, Alka S. Kushwah2, Shailendra N. Gaur3
1Department of Respiratory Allergy and Applied Immunology National Centre of Respiratory Allergy, Asthma and Immunology, V P
Chest Institute, University of Delhi, India
2V P Chest Institute, University of Delhi, Delhi, India
3Department of Respiratory Medicine, V P Chest Institute, University of Delhi, Delhi, India
Indoor air pollution and asthma in children at Delhi, India
The authors are thankful to the Ministry of Environment and Forest (MoEF), Government of India for financial grant for the study.
Abstract
Introduction: Several studies in developed countries have shown association between indoor air pollution and asthma in children.
The present research was undertaken to study this association at Delhi, India.
Material and methods: This study took place at Delhi, capital of India. Eight locations based on the source of pollution such as
industrial, residential and villages were included. Recording of the demographic prole and clinical examination of each child was
conducted at their residence. Indoor SO2, NO2 and SPM (suspended particulate matter) levels were measured by using Handy Air
Sampler (Low Volume Sampler).
Results: A total of 3104 children were examined of which 60.3% were male and 39.7% were female. 32.4% children were
exposed to environmental tobacco smoke. 31.5 % children’s families were using biomass fuels for cooking. History of respiratory
symptoms included cough (43.9%), phlegm production (21.9%), shortness of breath (19.3%) and wheezing (14.0%). 7.9% children
were diagnosed as having asthma, which was highest in industrial areas (11.8%), followed by residential (7.5%) and village areas
(3.9%). The mean indoor SO2, NO2 and SPM levels were 4.28±4.61 mg/m3, 26.70 ± 17.72 mg/m3 and 722.0 ± 457.6 mg/m3
respectively. Indoor SPM was the highest in industrial area followed by residential area and urban village area. Indoor SPM level
was signicantly (p < 0.001) higher in the asthmatic children’s houses.
Conclusion: This study suggests that industry plays an important role in increasing the concentration of indoor suspended par-
ticulate matter and occurrence of asthma in children in developing countries like India.
Key words: Indoor air pollution, SO2, NO2, SPM, asthmatic children, wheezing
Pneumonol Alergol Pol 2015; 83: 275–282
Introduction
Urban air pollution primarily due to suspen-
ded particulate matter (SPM), nitrogen dioxide
(NO2) and sulfur dioxide (SO2) is an environmen-
tal concern of many cities throughout the world.
It is responsible for causing serious respiratory
health problems like rhinitis, asthma, decreased
resistance to respiratory infections, chronic ob-
structive pulmonary disease (COPD), chronic
cough and phlegm production which lead to
premature death in the exposed population [1].
Delhi, India’s third largest city and its capital, is
also the third most polluted city in the country
[2]. The main source of suspended particulate in
Delhi are burning of fossil fuels, power stations,
vehicular transport, industries, domestic coal and
open biomass burning. Delhi’s annual average
concentration [3] of PM10 (particulate matter with
an aerodynamic diameter less than 10 mm) is the
highest among major Asian cities, and was between
3 and 4 times the Indian Standard in 2001−2004.
Indoor air quality (IAQ) has gained great
attention in the recent years, mainly due to the
large amount of time we spend indoors in modern
times. Indoor air pollution refers to chemical,
Pneumonologia i Alergologia Polska 2015, vol. 83, no. 4, pages 275–282
276 www.pneumonologia.viamedica.pl
biological and physical contamination of indoor
air. It may result in adverse health effects [4]. In
developing countries, the main source of indoor
air pollution is biomass smoke which contains
suspended particulate matter (SPM), nitrogen
dioxide (NO2), sulphur dioxide (SO2), etc. The
United States National Research Council (NRC)
reports [5] that people spend more than 80% of
their time indoors. Hence, they are exposed to
pollutants generated within the indoor environ-
ment, as well as those from the outdoors, which
may lead to increased exposure relative to that
outdoors [6]. Indoor pollutants depend on both in-
door and outdoor sources and removal processes,
such as air exchange or chemical reactions [6]. A
large number of indoor pollutants sources have
been identied which include tobacco smoking,
cooking with kerosene oil and wood burning [5, 6].
Combustion process is the main indoor source of
smaller particles and gases, with the vast majority
of them in the sub micrometer range, containing
a host of organic as well as inorganic materials.
Prevalence of asthma has increased during
the last decades in the countries worldwide.
Vehicle exhausts have been implicated for an
increased prevalence of wheeze, rhinitis, asthma
and other respiratory symptoms in children [7].
Few studies [8, 9] have reported air pollution as
a causative factor for asthma. In a 6-yr follow-up
study [8] among Japanese children a signicant
association was found between the annual ave-
rage concentration of nitrogen dioxide (NO2) and
the incidence of asthma.
There are several studies in developed coun-
tries showing the association between indoor air
pollution and asthma in children. There is lack of
data of indoor air pollutant level capital city of In-
dia. To the best of our knowledge there is no study
from India which correlates the relationship be-
tween indoor air pollutants (SO2, NO2 and SPM) and
asthma in children, hence this study was planned.
Material and methods
This study was undertaken at Delhi, capital
of India during 2004−2009 after ethical cle-
arance from the Institutional Ethics Committee.
According to Central Pollution Control Board
(CPCB) [10], India’s premier pollution monitoring
authority, the study areas were divided in eight
locations namely Ashok vihar (residential area),
Janakpuri (residential area), Nizamuddin (resi-
dential area), Siri Fort (residential area), Shahdara
(industrial area), Shahzada Bag (industrial area),
Dallupura (Village) and Jagatpur (Village). Central
Pollution Control Board has outdoor pollution
monitoring stations which measure daily pollu-
tants levels in each of these study areas except
villages. The 1 km area around the monitoring
station of CPCB was taken for study in each area.
Three colonies, one each representing the lower
(family with income less than 3000 rupees per
month), middle (family with 3000–5000 rupees
monthly income) and upper (family with inco-
me more than 10,000 rupees monthly income)
socioeconomic segments was randomly selected
for the survey. In villages, there was no class wise
distribution. Hundred houses with children aged
7−15 years from each socioeconomic class were
selected for survey and health checkup. Indoor
SO2, NO2 and SPM levels were monitored in 25%
houses from each area.
A questionnaire was developed on the basis
of ATS (American Thoracic Society) [11], BMRC
(British Medical Research Council) [12] and ISAAC
(The International Study of Asthma and Allergies
in Childhood) [13] questionnaires to detect the
presence of symptoms suggestive of asthma. The
questionnaire was also converted into Hindi. The
questionnaire included built-in demographic de-
tails like age and sex, food habits, smoking status
of child, smoking habits in the family, indoor
structure of home, fuel used for cooking, idea
about indoor air pollution, major chronic chest
symptoms (cough , phlegm, shortness of breath,
wheezing, chest illness). House visits were done
by the survey team and the questionnaire was
administered at the house itself. Examination of
the child, their pulmonary function test or PEFR,
was conducted. The diagnosis of asthma was
made by the physician examining the children,
based on the guidelines of ATS [11].
Spirometry test of children were done by the
use of an electronic portable Spirometer. Maximal
Expiratory Flow Volume (MEFV) curves were obta-
ined as per American Thoracic Society (ATS) 1995
recommendations [14]. In the children who could
not perform spirometry, Peak Expiratory Flow Rate
(PEFR) was obtained with a Wright’s Peak Flow Me-
ter. The highest of the three recordings was noted.
Indoor SO2, NO2 and SPM pollutants were
monitored by the methodology adopted as in
earlier studies [15, 16]. Indoor SO2, NO2 and
SPM levels were measured by using the Handy
Air Sampler or Low Volume Sampler (APM 810)
with a ow rate of 1 LPM (liter per minute) with
6-8 hours of sampling period. Handy Air Sampler
for indoor samples was positioned in the center
or corner of the room, with the inlet roughly
1 m above the ground level, corresponding with
Raj Kumar et al., Indoor air pollution and asthma
277
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the breathing height of the children. The indoor
sulfur dioxide and nitrogen dioxide concentration
were measured by West and Gaeke Modied Me-
thod [15] and Hochheiser Modied Method [16]
respectively.
The statistical analysis was performed with
SPSS statistical software. The groups were com-
pared for all variables using the Student t-test to
compare equality for means and the chi square test
to compare category value. The indoor SO2, NO2
and SPM levels were compared in the three areas
(industrial, residential and village) using analysis
of variance (ANOVA) followed by Post Hoc Bon-
ferroni multiple comparison test. The differences
were considered to be statistically signicant at
the p < 0.05 (two tailed test) level. Results are
presented as percentage and mean ± SD.
Results
There were 6613 houses which were survey-
ed and they had a total of 3104 children. Some of
the houses had more than one child. Consent for
study was given by 2513 houses having a total of
3104 children (60.3% males and 39.7% females).
The details of the ndings of the survey are shown
in Table 1 and Figure 1.
Over all a total of 7.9% (n = 244) children
were diagnosed as having asthma. Diagnosis
of asthma varied in different areas but was the
highest in Shahdara (14.2%) (Fig. 1). Asthma in
children was signicantly more frequent in in-
dustrial areas than residential and village areas
(Table 2). The number of children with asthma
was signicantly higher in upper socioeconomic
class compared to others (Table 1) with p value
< 0.001.The various characteristics of children
with and without asthma were compared and are
shown in Table 3.
Indoor SO2, NO2 and SPM level were me-
asured in 819 houses. The mean level of indoor
SO2, NO2 and SPM was 4.28 ± 4.61 mg/m3 (0.00
to 41.93 mg/m3), 26.70 ± 17.72 mg/m3 (0.00 to
141.13 mg/m3) and 722.0 ± 457.6 mg/m3 (80 to
2420 mg/m3) respectively. Concentration of indoor
air pollutants varied in each area (Fig. 1). Indoor
SPM and NO2 levels were signicantly higher in
industrial areas followed by residential and villa-
ge areas (Table 4). The factors affecting the levels
of indoor air pollutants are shown in Table 5. Use
of biomass fuel and occupancy per room of more
than 4 was signicantly associated with increased
SO2 levels. SPM levels were signicantly higher
with presence of smoker in family and increased
occupancy (> 4/room).
Mean indoor SPM levels were signicantly
higher in the houses of asthmatic children in all
areas (Fig. 2) and the difference was statistically
signicant. The mean indoor NO2 levels were hi-
gher in houses of asthmatic children in all areas
(Fig. 3) but the difference was not statistically
signicant. The SO2 levels were higher in houses
of asthmatic children in industrial and village
areas but the difference did not achieve statistical
signicance (Fig. 4).
Discussion
The major sources of air pollution in any city
like Delhi are industrial emissions, residential
heating and cooking, vehicular trafc and natural
sources, i.e., dust, wind. Suspended particulate
matter, sulfur dioxide and nitrogen dioxide are the
three major air pollutants in Delhi [17]. Indoor
coal combustion is the major source of indoor
particulate matter. The suspended particle con-
centration levels found in the kitchens are very
high. Indoor sources of NO2 include cigarette
smoke, gas and oil heaters and cookers which
often result in high indoor concentrations [18].
According to WHO air quality guidelines
(global update 2005) [19], the recommended
permissible limit for SO2 is 20 μg/m3 (24hr mean),
for NO2 is 40 μg/m3 (annual mean) and for SPM is
20 μg/m3 (24hr mean). Morand et al, [20] studied
the long-term exposure of air pollutants in Fran-
ce and found that mean levels of SO2, NO2 and
PM10 were 9.6 mg/m3, 40.6 mg/m3 and 23.8 mg/
m3 respectively. In London [21] the SO2 and PM10
concentrations were 21.2 ± 7.8 mg/m3 and 28.5 ±
13.7 mg/m3 respectively. In India, in Garhwal [22]
the mean level of indoor total suspended parti-
culate (TSP) during cooking by wood and shrubs
were found to be 4500 μg/m3. In another place in
India i.e. Pune [23], the 12−24 hours mean level
of indoor PM10 during cooking by wood was 2000
μg/m3. In Tamil Nadu (India) [24] the mean level
of indoor TSP during cooking by biomass was
500−2000 µg/m3. In the present study, the indoor
SO2, NO2 and SPM were found to be 4.28 ± 4.61
mg/m3, 26.70 ± 17.72 mg/m3 and 722.0 ± 457.6
mg/m3 respectively. Indoor SO2 concentration is
low in comparison to other countries which may
be explained probably by low overall outdoor
SO2 due to introduction of compressed natural
gas (CNG) fuel in vehicles since 2001. The high
levels of indoor NO2 and SPM are consistent with
the above studies.
The prevalence of asthma has increased
worldwide during the past two or three decades
Pneumonologia i Alergologia Polska 2015, vol. 83, no. 4, pages 275–282
278 www.pneumonologia.viamedica.pl
Table 1. General prole of children
Prole of Child Socioeconomic Status of Children Total
Lower Middle Upper Villages
Children studied 801 (25.8%) 821 (26.4%) 787 (25.4%) 695 (22.4%) 3104
Number of children diagnosed with asthma 73 (9.11%) 65 (7.91%) 79 (10.03%) 27 (3.88%) 244 (7.9%)
Male 63.5% 56.0% 58.4% 63.6% 60.3%
Female 36.5% 44.0% 41.6% 36.4% 39.7%
Vegetarian 81.1% 56.4% 40.9% 53.7% 58.2%
Non-Vegetarian 18.9% 43.6% 59.1% 46.3% 41.8%
Students 88% 98.9% 99.4% 98.5% 96.0%
Go to school by bus 35.1% 40.1% 59.1% 18.4% 39.0%
Go to school on foot 64.9% 59.9% 40.9% 81.6% 61.0%
History of smoking 1.1% 0.1% 0 0 0.3%
Children exposed to Environmental Tobacco Smoke (ETS) 50.3% 24.6% 20.7% 39.7% 32.4%
≤ 4 person occupancy per Room 42.2% 97.7% 98.2% 73.7% 78.1%
> 4 person occupancy per Room 57.8% 2.3% 1.8% 26.3% 21.9%
LP Gas used for cooking 22.3% 99.5% 99.9% 49.6% 68.5%
Biomass fuel used for cooking 77.7% 0.5% 0.1% 50.4 31.5%
Idea (knowledge) about indoor air pollution 11.5% 45.4% 71.3% 12.9% 36.0%
History of cough 54.2% 48.8% 47.5% 22.3% 43.9%
History of phlegm production 28.3% 25.1% 24.4% 7.9% 21.9%
History of shortness of breath 27.7% 20.2% 19.2% 8.5% 19.3%
History of wheezing 19.6% 14.6% 14.9% 5.9% 14.0%
Family history of chest diseases 4.7% 10.4% 15.9% 2.2% 8.5%
Airway obstruction 7.4% 7.2% 8.0% 6.3% 7.2%
especially in children and young adults. Ac-
cording to a study [25] conducted in Britain, in
England and Scotland, the prevalence of current
asthma in children increased from around 3%
in 1982 to 6% in 1985, and nearly reached 9%
in 1988. In Wales [26], current asthma increased
in children from 4% in 1973 to 9% in 1988. In a
study [27] in Chandigarh, India, the prevalence
of asthma in 9 to 20-years-olds schoolchildren
was 2.3%. In India, Mishra [28] also studied the
effect of indoor air pollution from biomass com-
bustion on prevalence of asthma in the elderly
and found the prevalence of asthma in more than
60-years-olds was around 8–10%. In our study the
prevalence of asthma was 7.9% (3.2% to 14.2%
in different areas). It was highest in industrial
areas (11.8%) followed by residential areas (7.4%)
and village areas (3.9%) and the difference was
statistically signicant. The area wise prevalence
of asthma was the lowest in Jagatpur & Dallupura
village with signicantly low pollution levels.
Jagatpur village is situated near the bank of river
Yamuna, agricultural elds and green biodiversity
park of Delhi.
There is a substantial epidemiological evi-
dence indicating a link between air pollution
and asthma morbidity including deterioration in
lung functions, increased number of emergency
department visits and hospital admissions [29].
A cross-sectional epidemiologic study [26] done
in six French cities found the association between
long-term exposure to air pollution and asthma.
Asthma was found to be positively related to an
increase in the exposure to SO2 (9.6 mg/m3) and
PM10 (23.8 mg/m3) but there was no consistent
positive association between NO2 (40.6 mg/m3)
Raj Kumar et al., Indoor air pollution and asthma
279
www.pneumonologia.viamedica.pl
Figure 1. Flow chart depicting study design and levels of SO2, NO2 and SPM in different study areas
Table 2. Asthma in children at industrial, residential and village areas
Area of Monitoring No. of children studied No. of children diagno-
sed with asthma
%age of children with
Asthma
Comparison of no. of asthmatic
children in different areas p-value
Industrial 831 98 11.8%
Industrial vs Residential < 0.001
Industrial vs Villages < 0.0001
Residential vs Villages < 0.01
Residential 1578 119 7.5%
Villages 695 27 3.9%
Total 3104 244 7.9%
Table 3. Comparison of various characteristics in children with asthma and without asthma
Children diagnosed
with Asthma
Children without
asthma
p-value
Male: Female 153: 91 1718: 1142 NS
Vegetarian: Non-vegetarian 86: 158 1209: 1650 NS
Smoking: No Smoker in family 89: 155 1015: 1845 NS
Fuel for cooking LPG: Biomass fuel 195: 45 2340: 520 NS
Kitchen with exhaust present: not present 144: 100 1467: 1393 p < 0.03
History of recurrent rhinitis present: absent 195: 49 640: 2220 p <0.0001
History of recurrent upper respiratory tract infection present: absent 176: 68 531: 2329 p <0.0001
Family history of asthma present: absent 48: 196 215: 2645 p <0.0001
Pneumonologia i Alergologia Polska 2015, vol. 83, no. 4, pages 275–282
280 www.pneumonologia.viamedica.pl
Table 5. Indoor air pollutants and factors inuencing them
Factor studied Status of
factor
Mean (± SD) SO2
levels (µg/m3)
Mean (± SD) NO2
levels (µg/m3)
Mean (± SD) SPM levels (mg/m3)
Smoker present in family No 4.46 ± 4.43 29.71 ± 20.75 660 ± 420
Yes 5.08 ± 7.49 32.64 ± 29.14 780 ± 470
p-value NS NS < 0.001
Occupancy per room £ 4 4.24 ± 4.81 28.91 ± 20.21 680 ± 430
> 4 6.06 ± 8.10 37.93 ± 34.36 830 ± 430
p-value < 0.0005 < 0.0002 < 0.0002
Biomass fuel used for
cooking
No 4.24 ± 4.28 30.26 ± 18.60 710 ± 430
Yes 5.52 ± 8.12 31.80 ± 33.94 690 ± 460
p-value < 0.020 NS NS
Figure 3. Comparison of mean NO2 levels in households having asth-
matic children versus households having non-asthmatic children in
different areas
Figure 2. Comparison of mean SPM levels in households having
asthmatic children versus households having non-asthmatic children
in different areas
Table 4. Comparison of levels of SO2, NO2 and SPM (suspended particulate matter) in different areas
Type of Area SO2 (µg/m3)
Mean ± SD
NO2 (µg/m3)
Mean ± SD
SPM (µg/m3)
Mean ± SD
Industrial (n = 212) 3.54 ± 3.95a35.88 ± 18.47a1080 ± 482.36a
Residential (n = 429) 5.22 ± 4.88b27.09 ± 16.38b705.6 ± 381.61b
Villages (n = 178) 2.88 ± 4.13a14.82 ± 11.64c334.9 ± 182.87c
F-ratio 20.885 83.295 187.649
P-value p < 0.0001 p < 0.0001 p < 0.0001
N.B. — variation in superscript indicates signicance of difference
and asthma. Modig et al. [30] studied the associa-
tion between the exposure to air pollutants and
increased risk of asthma in adults and found that
the association between asthma and measured
NO2 was weak and not signicant. However, in
a 6-yr follow-up study [8] among Japanese child-
ren a signicant association was found between
the annual average concentration of nitrogen
dioxide (NO2) and the incidence of asthma.
A study [31] in Hong Kong, China was con-
ducted to nd out association of air pollution
and asthma admission among children and it
concluded that the ambient levels of PM10 and
NO2 but not SO2, were associated with childhood
Raj Kumar et al., Indoor air pollution and asthma
281
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Table 6. Factors affecting the occurrence of childhood asthma*
Variable Driver rank Importance Standardized estimate Impact
Years of breast-feeding 1 52% −1.5679 −
Number of sisters 2 9% −0.2739 −
Industrial area 3 9% 0.2546 +
Air quality in the locality 4 6% 0.1776 +
Number of brothers 5 6% −0.1667 −
Socioeconomic status 6 5% 0.1511 +
Child suffering from any disease 7 5% 0.1437 +
Family history 8 3% 0.0907 +
Food habit — vegetarian 9 3% −0.0902 −
Animals & pets 10 3% 0.0756 +
*Method used: Logistic regression with variable selection technique; Signicant level < 0.10 (indicating about 90% probability of the impact of the driver on the
occurrence of asthma)
Figure 4. Comparison of mean SO2 levels in households having asth-
matic children versus households having non-asthmatic children in
different areas
asthma hospital admissions. In a longitudinal
study of 150 preschool children with asthma
(Baltimore Indoor Environment Study of Asthma
in Kids [BIESAK] Study), the impact of indoor
ne (PM2.5) and coarse PM (PM2.5–10) on asth-
ma was investigated [32]. The study found that
indoor coarse PM concentrations were associated
with substantial increases in asthma symptoms
and the ne PM were also positively associated
with increased respiratory symptoms and rescue
medication use. These studies are consistent
with our study in which the diagnosed asthma in
children was associated with the highest levels
of indoor suspended particulate matter (SPM)
(p = 0.001) and NO2 (p = 0.036). Indoor SPM was
signicantly higher in the houses of asthmatic
children of industrial (p = 0.001), residential
(p = 0.001) and village (p = 0.019) areas.
We also did the statistical analysis of the
data using logistic regression analysis with va-
riable selection technique and found the drivers
responsible in our study cohort for occurrence of
asthma in children. These have been depicted in
Table 6. Noticeably, the number of years of breast
feeding was the most important driver which
had a protective inuence on the occurrence of
asthma in children.
Inability to obtain 24 hour mean values of
indoor air pollutants remained a limitation of
our study.
Conclusion
The present research was carried out to study
the relationship between indoor air pollutants level
and asthma in children. Both indoor SPM levels
and occurrence of asthma in children were found
to be higher in industrial areas compared to resi-
dential and urban village areas. Further, the houses
with asthmatic children in all these areas had still
higher levels of indoor SPM as compared to houses
without asthmatic children and the difference was
statistically signicant. Hence, this study suggests
that industry plays an important role in increasing
the concentration of indoor suspended particulate
matter, and also increased occurrence of asthma in
children in developing countries like India.
Conict of interest
The authors declare no conict of interest.
Pneumonologia i Alergologia Polska 2015, vol. 83, no. 4, pages 275–282
282 www.pneumonologia.viamedica.pl
References:
1. Seiber JN. Toxic air contaminants in urban atmospheres:
experience in California. Atmospheric Environment 1996; 30:
751−756.
2. World Health Organization. Urban outdoor air pollution da-
tabase, by country and city (corrected version) 2011. [Inter-
net]. 6 October 2012. Available from: http://www.who.int/
entity/phe/health_topics/outdoorair/databases/OAP_databa-
se.xls; 15.03.2015.
3. Health Effects Institute. Health effects of outdoor air pollution
in developing countries of Asia: A literature review, Special
Report 15, 2004. [Internet]. 7 October 2012. Available from:
http://pubs.healtheffects.org/view.php?id=3; 15.03.2015.
4. Glossary of Environment Statistics, Studies in Methods, Series
F, No. 67, United Nations, New York, 1997. Available at http://
stats.oecd.org/glossary/detail.asp?ID=1336; 15.03.2015.
5. Wadden RA, and Scheff PA. Indoor Air Pollution. Wiley Inter-
science, New York 1983: 52−78.
6. He C, Morawska, L, Hitchins J and Gilbert D. Contribution
from indoor sources to particle number and mass concentra-
tions in residential houses. Atmospheric Environment 2004:
38; 3405−3415.
7. Ciccone G, Forastiere F, Agabiti N et al. Road trafc and adverse
respiratory effects in children. Occup Environ Med 1998: 55;
771−778.
8. Shima M, Nitta Y, Ando M, Adachi M. Effects of air pollution
on the prevalence and incidence of asthma in children. Arch
Environ Health 2002: 57; 529−535.
9. Edward J, Walters S, Grifths RK. Hospital admissions for asth-
ma in preschool children: relationship to major roads in Bir-
mingham, United Kingdom. Arch Environ Health 1994: 49;
223−227.
10. Central Pollution Control Board. Ministry of Environmental
Health and Forests. Government of India, Available from:
http://cpcb.nic.in/; 15.03.2015.
11. Ferris BG. Epidemiology standardization project. Am Rev Re-
spir Dis 1978; 118: 1−53.
12. Medical Research Council — standardized questionnaires on
respiratory symptoms. Br Med J 1960; 2: 1665.
13. Keil U, weiland SK, Duhme H, Chambless L. The International
study of asthma and allergies in childhood (ISAAC): objectives
and methods; result from German ISAAC centers concerning
trafc density and wheezing and allergic rhinitis. Toxicol Lett
1996; 86: 99−103.
14. ATS recommendation. Standardization of spirometry. Am J
Respir Crit Med 1995; 152: 1107−1136.
15. West PW, Gaeke GC. Fixation of sulfur dioxide as Sulpitomer-
curate III and subsequent calorimetric determination. Anal
Chem 1956; 28: 1816.
16. Jacab MB, Hochheiser S. Continous sampling and ultra-micro de-
termination of nitrogen dioxide in air. Anal Chem 1958; 30: 426.
17. Singh MP, Goyal P, Panwar TS, Aggarwal P, Nigam S. Predicted
and observed concentrations of SO2, SPM and NOx over Delhi.
Atmospheric Environment 1990; 24A: 783−788.
18. Wardlaw AJ. The role of air pollution in asthma. Clin Exp
Allergy 1993; 23: 81−96.
19. World Health Organization 2006. WHO Air quality guideli-
nes for particulate matter, ozone, nitrogen dioxide and sulfur
dioxide. Global update 2005 Summary of risk assessment. [In-
ternet] 5 October 2012. Available from: http://whqlibdoc.who.
int/hq/2006/WHO_SDE_PHE_OEH_06.02_eng.pdf; 15.03.2015.
20. Morand CP, Charpin D, Raherison C et al. Long-term exposure to
background air pollution related to respiratory and allergic he-
alth in schoolchildren. Clin Exp Allergy 2005; 35: 1279−1287.
21. Hajat S, Haines A, Atkinson RW, Bremner SA, Anderson HR, Em-
berlin J. Association between air pollution and daily consultations
with general practitioners for allergic rhinitis in London, United
Kingdom. American Journal of Epidemiology 2001; 153: 704−714.
22. Saxena S, Prasad R, Pal RC, Joshi V. Patterns of daily expo-
sure to TSP and CO in the Garhwal Himalaya. Atmospheric
Environment 1992; 26A: 2125−2134.
23. Smith KR, Liu Y. Indoor air pollution in developing countries.
In: Samet JM (ed.) Epidemiology of lung cancer. New York
1994: 151−183.
24. Balakrishnan K, Parikh J, Sankar S et al. Daily average expo-
sures to respirable particulate matter from combustion of bio-
mass fuels in rural households of southern India. Environmen-
tal Health Prospect 2002; 11: 1069−1075.
25. Rona RJ, Chinn S, Burney PGJ. Trends in the prevalence of
asthma in Scottish and England primary school children
182−92. Thorax 1995; 50: 992−993.
26. Burr ML, Butland BK, King S, Vaughan Villiams E. Changes in
asthma prevalence: two surveys 15 years apart. Arch Dis Child
1989; 64: 1452−1456.
27. Gupta, D, Aggarwal AN, Kumar J, Jindal SK. Prevalence of
bronchial asthma and association with environmental tobacco
smoke exposure in adolescent school children in Chandigarh,
North India. J Asthma 2001; 38: 501−507.
28. Mishra V. Indoor air pollution from biomass combustion on
prevalence of asthma in the elderly. Environ Health Prospect
2003; 111: 71−77.
29. Air quality guidelines for Europe. WHO Regional Publications,
European Series No. 23, 1987; 315−326.
30. Modig L, Jarvholm B, Ronnmark E et al. Vehicle exhaust expo-
sure in an incident case-control study of adult asthma. Eur
Respir J 200; 28: 75−81.
31. Lee SL, Wong WHS, Lau YL. Association between air pollution
and asthma admission among children in Hong Kong. Clin Exp
Allergy 2006; 36: 1138−1146.
32. Breysse PN, Diette GB, Matsui EC, Butz AM, Hansel NN,
McCormack MC. Indoor air pollution and asthma in children.
Proc Am Thorac Soc. 2010; 7: 102−116. doi: 10.1513/pats.
200908-083RM.
